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EHA 2026 | Targeting hepcidin in polycythemia vera and myelofibrosis
Ruben Mesa, MD, Levine Cancer Institute, Atrium Health Wake Forest Baptist Comprehensive Cancer Center, Winston Salem, NC, discusses the evolving understanding of iron regulation and hepcidin biology in myeloproliferative neoplasms (MPNs), highlighting the role of hepcidin in both myelofibrosis and polycythemia vera (PV). Dr Mesa notes that modulating hepcidin levels may help alleviate anemia in myelofibrosis and reduce phlebotomy requirements in PV, potentially improving symptom control and disease management. This interview took place at the 31st Congress of the European Hematology Association (EHA) in Stockholm, Sweden.
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Transcript
Hepcidin is involved with iron regulation and iron metabolism and is also a part of the kind of inflammatory response. And what I’m able to discuss at this year’s EHA meeting is that it’s really relevant in both directions. So one, there’s elevation of hepcidin in patients with myelofibrosis and there are agents which are being developed that may help to decrease that hepcidin and then helps to alleviate some of the anemia of chronic disease so specifically to try to improve anemia for patients with myelofibrosis...
Hepcidin is involved with iron regulation and iron metabolism and is also a part of the kind of inflammatory response. And what I’m able to discuss at this year’s EHA meeting is that it’s really relevant in both directions. So one, there’s elevation of hepcidin in patients with myelofibrosis and there are agents which are being developed that may help to decrease that hepcidin and then helps to alleviate some of the anemia of chronic disease so specifically to try to improve anemia for patients with myelofibrosis. On the flip side there are agents, both rusferitide as well as sapablursen, where I’m one of the co-investigators on the trial being presented here at EHA, that are working to try to decrease hepcidin levels through a couple different mechanisms for patients with polycythemia vera. So in polycythemia vera, we have really the opposite problem of myelofibrosis, too few red blood cells in myelofibrosis. In polycythemia vera, really too many red blood cells. And then by the inhibition of hepcidin, or using hepcidin mimetics, I should say, for PV, we’re then able to decrease that erythrocytosis, allow patients to become phlebotomy independent. The importance of that is that one, it allows them to have a less iron deficiency that is created by the process of phlebotomies. And iron deficiency may contribute to a variety of the difficult symptoms that patients have with PV. So an important new kind of lever in both directions, both for MF and for PV, with really modulation of hepcidin.
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